ABSTRACT
Eighty subjects were selected for this study, 65 of them were patients of liver cirrhosis [43 males and 22 females] and 15 of them were normal individuals as a control group [11 males and 4 females]. All the 80 subjects were subjected to full clinical assessment, biochemical liver profile, kidney profile, abdominal ultrasonography and estimation of plasma prostaglandin E2 [PGE2]. It was found that PGE2 was significantly increased in cirrhotic patients and this increase was more in ascitic than non-ascitic patients and more in Child C patients than in other Child classes, but there is evident marked significant drop in PGE2 level with the development of hepatorenal syndrome [HRS]. It was concluded that the increase of the vasodilator PGE2 in cirrhotic patients is a protective factor against the catastrophic effect of increased vasoconstrictor mediators characteristic of liver cirrhosis and the drop of PGE2 could be a causative factor in pathogenesis of HRS as it drops leaving the kidney under the vigorous effect of vasoconstrictors. The study postulated a new formula which might be more sensitive for the prediction of HRS